Alzheimer Brain Destroyed By Too Many Blood Vessels

The blood vessel growth (neo-angiogenesis) produces a breakdown of the blood-brain barrier, the densely interwoven cell-network that allows oxygenated blood to reach brain tissue while blocking harmful substances, such as viruses.

Researchers at the University of British Columbia (UBC) may have discovered that a profusion of blood vessels may explain how Alzheimer's disease destroys the brain.

Although previous Alzheimer's research concentrated mainly on the death of cells in the walls of blood vessels or in brain tissue, a new study led by Professor Wilfred Jefferies (pictured) in UBC's Michael Smith Laboratories revealed that the neurodegenerative disease might possibly be caused by the propagation of cells in blood vessel walls.

When Jefferies and colleagues examined brain tissue from mouse models of Alzheimer's disease, they discovered almost twice the density of capillaries compared to normal mice. They also discovered a comparably higher density of capillaries in human brain samples of people who died of Alzheimer's compared with samples of humans who didn't have the condition.

Jefferies theory, that the profusion of blood vessels is stimulated by amyloid beta, a 'trademark' protein fragment of Alzheimer's disease was published recently.

The blood vessel growth (neo-angiogenesis) produces a breakdown of the blood-brain barrier, the densely interwoven cell-network that allows oxygenated blood to reach brain tissue while blocking harmful substances, such as viruses.

Jefferies, who works in the departments of microbiology and immunology, medical genetics and zoology, and is also a member of the Biomedical Research Centre and the Brain Research Centre, explains:

"When the blood vessels grow, the cells of the vessel walls propagate by dividing. In the process of splitting into two new cells, they become temporarily rounded in shape, and that undermines the integrity of the blood-brain barrier, potentially allowing harmful elements from outside the brain to seep in."

The deterioration of the barrier might consequently facilitate depositing of amyloid beta, which accumulates around neurons eventually killing them. Earlier research acknowledged the "leakiness" of the barrier, but assumed that it was caused by the death of blood vessels and not their growth.

Jefferies also observed an intriguing similarity with the "wet" form of age-related macular degeneration, in which blood vessels grow behind the retina and then leak blood and fluid, resulting in hemorrhaging, swelling, and formation of scar tissue.

In a concluding statement Jefferies said:

"Given the new link between both conditions, the next logical step in the treatment of Alzheimer's disease would be to look for treatments that specifically target blood vessel growth."